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Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure
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Number of Authors: 1462020 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 11, no 1, article id 163Article in journal (Refereed) Published
Abstract [en]

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies.

Place, publisher, year, edition, pages
2020. Vol. 11, no 1, article id 163
National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
URN: urn:nbn:se:du-31615DOI: 10.1038/s41467-019-13690-5ISI: 000511898900014PubMedID: 31919418Scopus ID: 2-s2.0-85077697294OAI: oai:DiVA.org:du-31615DiVA, id: diva2:1385779
Available from: 2020-01-15 Created: 2020-01-15 Last updated: 2020-03-12

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